| Linden (LTP/LTD in hippocampus) | Huganir (Ligand-gated channels) | Shan (Neural Induction) | Anatomy | [blank] |
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After induction of LTP, GluR1 tagged with GFP shows greater localization to spines.
Describe one experiment that supports the hypothesis that LTP at the CA3-CA1 synapse is mediated by an increase in AMPARs at the postsynaptic membrane.
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You can generate an antibody against subunit a1, then use co-IP to pull down for it and examine which subunits are pulled down with it.
Name one method of determining what combinations of subunits endogenously form a GABA receptor with subunit a1.
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Dissociated ectodermal cells form neurons, but intact ectoderm from the animal pole gives rise to epidermis; providing dissociated cells with BMP causes epidermis to form, and providing intact tissue with BMP inhibitors leads to neurons.
What is the “default” state for ectoderm? How can this be changed?
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Silent synapses have NMDARs but no AMPARs, so they do not transmit a signal upon glutamate release until LTP leads to the insertion of AMPARs. In the “free lunch” experiment, synapses that are silent when held at -60 mV are active when held at +30 mV, and this is blocked by AP-V.
What is a “silent”/“deaf” synapse? Describe an experiment that demonstrates their existence.
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The ACh receptors in cows and Torpedo show different conductances. Chimeras were generated by swapping regions between the two to which swap could cause the conductances to switch. In doing so, the ion pore was localized to TM2.
Which TM domain of the acetylcholine receptor contains the ion pore? Describe how the location was found.
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The most anterior end is characterized by Wnt inhibitors like Cerberus. Structures giving rise to the more posterior parts of the brain are patterned by BMP inhibitors like Noggin. The spinal cord is patterned through FGF and RA signals.
Describe the factors that pattern the A-V neural axis.
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GluR2. Combinations of subunits including GluR2, but not ones lacking it, give a linear I-V curve matching that of the endogenous AMPAR. This is due to an R where other AMPAR subunits have a Q; this difference is not due to a genomic difference but RNA editing of a single nucleotide.
Which AMPAR subunit gives the receptor a linear I-V curve? Describe how this was determined. Which residue in this subunit is responsible? What's unique about how this residue is coded?
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In both LTP and LTD, Ca is fluxed through NMDARs and binds calmoldulin. During LTD, low Ca influx is only capable of activating calcineurin, which activates the phosphatase PP-1 leading to dephosphoryation and LTD. During LTP, larger Ca influx activates CaMKII, whose phosphorylating activity is able to outcompete the phosphatase activity of PP-1.
Explain how Ca influx can be responsible for both LTP and LTD. Mention two components shared by both processes and one unique one for each.
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The hydrophobicity plot of GluR1 suggests that it has 4 TMs. This would mean that the N- and C-termini would be on the same side of the plasma membrane; however, the N-terminal has glycosylation sites (must be extracellular) and the C-terminal has phosphorylation sites (must be intracellular). It was then found that the putative “TM2” did not pass all the way through the membrane, giving 3 proper TMs.
Why was it believed that GluR1 had four transmembrane domains? What proved this belief incorrect? Briefly describe its actual topology.
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Transplanting mesoderm just adjacent to the dorsal blastopore lip to a second embryo caused the formation of a secondary neural tube. The organizer secretes BMP inhibitors like Chordin, Noggin, and Follistatin.
Describe the experiment that identified the organizer in Xenopus. What factors does it secrete?
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